title: Microbial translocation in HIV infection is associated with dyslipidemia, insulin resistance, and risk of myocardial infarction.
abstract: OBJECTIVE
  Microbial translocation has been suggested to be a driver of immune activation and inflammation. It is hypothesized that microbial translocation may be related to dyslipidemia, insulin resistance, and the risk of coronary heart disease in HIV-infected individuals.
  
  
  METHODS
  Cross-sectional study of 60 HIV-infected patients on combination antiretroviral therapy with viral suppression >2 years and 31 healthy age-matched controls.
  
  
  METHODS
  Lipopolysaccharide (LPS) was analyzed by limulus amebocyte lysate colorimetric assay. Lipids, including cholesterol, low-density lipoprotein (LDL), and triglycerides, were measured. Glucose metabolism was determined using an oral glucose tolerance test. Body composition was determined using whole-body dual-energy x-ray absorptiometry scans and magnetic resonance imaging. The Framingham risk score was used to assess risk of cardiovascular disease and myocardial infarction.
  
  
  RESULTS
  HIV-infected patients had higher level of LPS compared with controls (64 pg/mL vs. 50 pg/mL, P = 0.002). Likewise, HIV-infected patients had higher triglycerides, LDL, and fasting insulin as well as evidence of lower insulin sensitivity compared with controls. Among HIV-infected patients, high LPS was associated with a higher level of triglycerides and LDL and with lower insulin sensitivity. Importantly, among HIV-infected patients, high LPS was associated with a higher Framingham risk score.
  
  
  CONCLUSIONS
  HIV-infected patients with suppressed viral replication had increased level of microbial translocation as measured by LPS. LPS was associated with cardiometabolic risk factors and increased Framingham risk score. Hence, the gastrointestinal mucosal barrier may be a potential therapeutic target to prevent dyslipidemia and future cardiovascular complications in HIV infection.
authors.affiliation: *Department of Infectious Diseases, Rigshospitalet, University Hospital of Copenhagen, Copenhagen, Denmark; †Centre of Inflammation and Metabolism, Rigshospitalet, University Hospital of Copenhagen, Copenhagen, Denmark; ‡Department of Infectious Diseases, Oslo University Hospital, Oslo, Norway; §Department of Radiology, Rigshospitalet, University Hospital of Copenhagen, Copenhagen, Denmark; and ‖Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
authors.forename: Karin K
authors.initials: KK
authors.lastname: Pedersen
authors.forename: Maria
authors.initials: M
authors.lastname: Pedersen
authors.forename: Marius
authors.initials: M
authors.lastname: Trøseid
authors.forename: Julie C
authors.initials: JC
authors.lastname: Gaardbo
authors.forename: Tamara T
authors.initials: TT
authors.lastname: Lund
authors.forename: Carsten
authors.initials: C
authors.lastname: Thomsen
authors.forename: Jan
authors.initials: J
authors.lastname: Gerstoft
authors.forename: Dag
authors.initials: D
authors.lastname: Kvale
authors.forename: Susanne D
authors.initials: SD
authors.lastname: Nielsen
mesh_terms: D015502:Absorptiometry, Photon; D000328:Adult; D000368:Aged; D000818:Animals; D044966:Anti-Retroviral Agents / Q000627:therapeutic use; D023241:Antiretroviral Therapy, Highly Active / Q000379:methods; D018988:Bacterial Translocation; D001823:Body Composition; D003430:Cross-Sectional Studies; D050171:Dyslipidemias / Q000453:epidemiology* / Q000473:pathology; D005260:Female; D005951:Glucose Tolerance Test; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy / Q000473:pathology; D006801:Humans; D007333:Insulin Resistance; D008033:Limulus Test; D008055:Lipids / Q000097:blood; D008070:Lipopolysaccharides / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology* / Q000473:pathology
chemical_list: D044966:Anti-Retroviral Agents; D008055:Lipids; D008070:Lipopolysaccharides